A Novel Indicator to Correct for Individual Reported Heterogeneity. An Application to Self-Evaluation of Later-Life Depression.

Program evaluations often investigate complex or multi-dimensional constructs, such as individual opinions or attitudes, by means of ratings. A different interpretation of the same question may affect cross-country comparability, leading to the Differential Item Functioning problem. Anchoring vignettes were introduced in the literature as a way to adjust self-evaluations from this interpersonal incomparability. In this paper, we first introduce a new nonparametric solution to analyse anchoring vignette data, recoding a variable based on a rating scale to a new corrected-variable that guarantees comparability in any cross-country analysis. Then, we exploit the flexibility of a mixture model introduced to account for uncertainty in the response process (the CUP model) to test if the proposed solution is effectively able to remove this reported heterogeneity. This solution is easy to construct and has important advantages compared with the original nonparametric solution adopted with anchoring vignette data. The novel indicator is applied to investigate self-reported depression in an old population. Data that will be analysed come from the second wave of the Survey of Health, Ageing and Retirement in Europe, collected in 2006/2007. Results highlight the need of correcting for reported heterogeneity comparing individual self-evaluations. Once interpersonal incomparability resulting from the different uses of response scales is removed from the self-assessments, some estimates are reversed in magnitude and signs with respect to the analysis of the collected data.

Pilot Study to Investigate the Benefits of the InnoSpire Go Mesh Nebulizer Compared to Jet Nebulizers in the Treatment of Stable COPD.

Background: Nebulizers are widely used for the delivery of aerosols to patients with chronic obstructive pulmonary disease (COPD). The InnoSpire Go mesh nebulizer has been designed to improve upon the ease of use and convenience of existing nebulizers for the treatment of COPD. Methods: This was a pilot, single-center, randomized, open-label crossover study conducted over 2 months to investigate the use of the InnoSpire Go mesh nebulizer compared to the patient's own compressor driven jet nebulizer in ambulatory patients with stable COPD. Patient preference was assessed at the end of the study; quality of life, symptom scores, treatment time, and satisfaction were assessed at multiple points during the study. Results: Data for 17 patients were eligible for analysis, patients had a mean age of 64.6 years, and 64.7% were graded 3 on the modified Medical Research Council dyspnea scale. All patients preferred the InnoSpire Go mesh nebulizer over their own compressor driven jet nebulizer (p < 0.001). Nebulization of study drugs using the InnoSpire Go mesh nebulizer was associated with statistically significant increases in health-related quality of life over baseline (Dyspnea p = 0.003, Emotion p = 0.043, Mastery p = 0.011). A mixed model analysis of Borg dyspnea scores before and after exercise showed significantly (p = 0.043) lower scores for the InnoSpire Go mesh nebulizer compared with the compressor driven nebulizers. Patient satisfaction was statistically significantly higher for each of 10 questions covering ease of use, confidence, burden of use, satisfaction, and how well the device fit into their lifestyle. Treatment time was significantly shorter with the InnoSpire Go mesh nebulizer (p = 0.003). Conclusions: Patients preferred and were more satisfied with the InnoSpire Go mesh nebulizer. Nebulization of study drugs using the InnoSpire Go mesh nebulizer resulted in improved quality of life compared with baseline, and treatments were delivered in a shorter period than the compressor driven jet nebulizers. Clinical Trial Registration number: ClinicalTrials.gov: NCT03933462.

Estradiol prevented intestinal ischemia and reperfusion-induced changes in intestinal permeability and motility in male rats.

OBJECTIVES: Ischemia and reperfusion (I/R) in the intestine could lead to severe endothelial injury, compromising intestinal motility. Reportedly, estradiol can control local and systemic inflammation induced by I/R injury. Thus, we investigated the effects of estradiol treatment on local repercussions in an intestinal I/R model. METHODS: Rats were subjected to ischemia via the occlusion of the superior mesenteric artery (45 min) followed by reperfusion (2h). Thirty minutes after ischemia induction (E30), 17ß-estradiol (E2) was administered as a single dose (280 µg/kg, intravenous). Sham-operated animals were used as controls. RESULTS: I/R injury decreased intestinal motility and increased intestinal permeability, accompanied by reduced mesenteric endothelial nitric oxide synthase (eNOS) and endothelin (ET) protein expression. Additionally, the levels of serum injury markers and inflammatory mediators were elevated. Estradiol treatment improved intestinal motility, reduced intestinal permeability, and increased eNOS and ET expression. Levels of injury markers and inflammatory mediators were also reduced following estradiol treatment. CONCLUSION: Collectively, our findings indicate that estradiol treatment can modulate the deleterious intestinal effects of I/R injury. Thus, estradiol mediates the improvement in gut barrier functions and prevents intestinal dysfunction, which may reduce the systemic inflammatory response.

Estradiol prevented intestinal ischemia and reperfusion-induced changes in intestinal permeability and motility in male rats

OBJECTIVES: Ischemia and reperfusion (I/R) in the intestine could lead to severe endothelial injury, compromising intestinal motility. Reportedly, estradiol can control local and systemic inflammation induced by I/R injury. Thus, we investigated the effects of estradiol treatment on local repercussions in an intestinal I/R model. METHODS: Rats were subjected to ischemia via the occlusion of the superior mesenteric artery (45 min) followed by reperfusion (2h). Thirty minutes after ischemia induction (E30), 17β-estradiol (E2) was administered as a single dose (280 μg/kg, intravenous). Sham-operated animals were used as controls. RESULTS: I/R injury decreased intestinal motility and increased intestinal permeability, accompanied by reduced mesenteric endothelial nitric oxide synthase (eNOS) and endothelin (ET) protein expression. Additionally, the levels of serum injury markers and inflammatory mediators were elevated. Estradiol treatment improved intestinal motility, reduced intestinal permeability, and increased eNOS and ET expression. Levels of injury markers and inflammatory mediators were also reduced following estradiol treatment. CONCLUSION: Collectively, our findings indicate that estradiol treatment can modulate the deleterious intestinal effects of I/R injury. Thus, estradiol mediates the improvement in gut barrier functions and prevents intestinal dysfunction, which may reduce the systemic inflammatory response.

Acute lung injury induced by intestinal ischemia and reperfusion is altered in obese female mice.

RATIONAL: Acute lung injury (ALI) is a common complication after intestinal ischemia and reperfusion (I/R) injury that can lead to acute respiratory distress syndrome (ARDS). We have previously demonstrated that females are protected against lung damage induced by intestinal I/R through an estrogen mediated mechanism. OBJECTIVES: To investigate the effect of obesity on ALI induced by intestinal I/R in female mice. METHODS: C57Bl/6 female mice were fed with a standard low-fat diet (SD) or a high-fat diet (HFD) for 9 weeks. Intestinal I/R injury was induced by a 45 min occlusion of the mesenteric artery followed by 2 and 24 h of reperfusion. RESULTS: Significant increase in lung myeloperoxidase expression (MPO) and neutrophil numbers of SD and HFD mice occurred at 2 h and 24 h of reperfusion. Furthermore, HFD mice presented a significant increase in lung eosinophil peroxidase (EPO) expression and eosinophil numbers compared to SD mice. Lung wet/dry weight ratio was significantly greater in HFD mice at 2 and 24 h of reperfusion, accompanied by a significant increase in the expression of inducible NO in the lung tissue and a significant decrease in arterial oxygen saturation at 24 h of reperfusion relative to SD mice. CONCLUSION: Obesity predisposes female mice to increased pulmonary oedema and deterioration in gas exchange, which is accompanied by an increase in iNOS expression in the lung.

Estradiol mediates the long-lasting lung inflammation induced by intestinal ischemia and reperfusion.

BACKGROUND: Lung inflammation is one of the main consequences of intestinal ischemia reperfusion (intestinal IR) and, in severe cases, can lead to acute respiratory distress syndrome and death. We have previously demonstrated that estradiol exerts a protective effect on lung edema and cytokine release caused by intestinal IR in male rats. MATERIALS AND METHODS: We investigated the role of estradiol on the generation of interleukin (IL)-1ß, IL-10, vascular endothelial growth factor (VEGF), and cytokine-induced neutrophil chemoattractant 1 (CINC-1) in a female rat model of intestinal IR. Blood and bone marrow leukocytes were also quantified. Seven-days-ovariectomized rats were subjected to intestinal IR by occlusion of the superior mesenteric artery for 45 min. After reperfusion of the tissue for 2 h, the rats were sacrificed. Lung tissue was collected, cultured for 24 h and assayed. RESULTS: We observed a significant increase in serum levels of IL-10, CINC-1, uric acid and circulating, but not bone marrow, leukocyte numbers. In addition, intestinal IR induced a significant increase in the ex-vivo lung levels of IL-1ß, IL-10, and VEGF. Treatment with 17ß-estradiol before the induction of intestinal IR prevented the systemic release of IL-10, CINC-1, and uric acid, but it did not affect the leukocytosis. In addition, 17ß-estradiol significantly prevented the ex-vivo release of IL-1ß and VEGF from lung tissue. CONCLUSIONS: We demonstrated that intestinal IR interferes with lung homeostasis, priming the tissue to generate proinflammatory mediators for at least 24 h postischemia. Furthermore, our data confirm that the inflammatory responses caused by intestinal IR are estradiol mediated.

Estradiol Modulates Local Gut Injury Induced by Intestinal Ischemia-Reperfusion in Male Rats.

Intestinal ischemia and reperfusion (I/R) triggers a systemic inflammatory response characterized by leukocyte mobilization from the bone marrow, release of cytokines to the circulation, and increased microvascular permeability, leading to high mortality. Females have shown attenuated inflammatory response to trauma when compared with males, indicating a role for female sex hormones in this process. Here, we have evaluated the effect of estradiol on the local gut injury induced by I/R in male rats. I/R was induced by the clamping of the superior mesenteric artery for 45 min, followed by 2 h of reperfusion. A group received 17ß-estradiol (280 µg/kg, i.v., single dose) at 30 min of ischemia. Morphometric analysis of the gut showed I/R induced a reduction of villous height that was prevented by estradiol. White blood cells, notably granulocytes, were mobilized from the circulation to the intestine by I/R, which was also prevented by estradiol treatment. Groups had the intestine wrapped in a plastic bag to collect intestinal fluid, where leukocytes count, TNF-α, and IL-10 levels were increased by I/R. Serum chemokines (CINC-1, MIP-1α, MIP-2), ICAM-1 expression in the mesenteric tissue, and neutrophils spontaneous migration measured in vitro were also increased after I/R. Estradiol treatment reduced leukocytes numbers and TNF-α on intestinal fluid, serum chemokine release and also downregulated MIP-1α, MIP-2 gene expression, and spontaneous in vitro neutrophil migration. In conclusion, estradiol blunts intestinal injury induced by I/R by modulating chemokines release and leukocyte trafficking.

The Challenge and Opportunity of Parental Involvement in Juvenile Justice Services.

The active involvement of parents - whether as recipients, extenders, or managers of services - during their youth's experience with the juvenile justice system is widely assumed to be crucial. Parents and family advocacy groups note persisting concerns with the degree to which successful parental involvement is achieved. Justice system providers are highly motivated and actively working to make improvements. These coalescing interests provide a strong motivation for innovation and improvement regarding family involvement, but the likely success of these efforts is severely limited by the absence of any detailed definition of parental involvement or validated measure of this construct. Determining whether and how parental involvement works in juvenile justice services depends on the development of clear models and sound measurement. Efforts in other child serving systems offer guidance to achieve this goal. A multidimensional working model developed with parents involved in child protective services is presented as a template for developing a model for parental involvement in juvenile justice. Features of the model requiring changes to make it more adaptable to juvenile justice are identified. A systematic research agenda for developing methods and measures to meet the present demands for enhanced parental involvement in juvenile justice services is presented.